Atrial fibrillation (AF) involves rapid and chaotic beating of the individual fibers of the heart muscle such that synchronous contraction is not maintained. This inevitably results in that part of the heart ceasing to pump blood, which in turn can lead to embolic stroke. Atrial fibrillation is characterized by the presence of multiple reentrant circuits that may be active simultaneously, precluding the synchronous activation of enough atrial myocardium to generate an identifiable p wave or coordinated atrial contraction. Either a sinus impulse or a stable atrial flutter reentrant circuit (flutter wave) may degenerate into the multiple reentrant circuits (multiple wavelets) characteristic of atrial fibrillation. [Cox et al., J. Thoracic. Cardiovas. Surg. 101:402-405 (1991)].
Degeneration of the stable activation patterns of sinus rhythm and atrial flutter into atrial fibrillation is enhanced when there is a disparity in the local refractory periods of closely approximated regions of atrial myocardium. However, atrial geometry, atrial anisotropy, and histopathologic changes in the atrial myocardium may also predispose to both atrial flutter and atrial fibrillation.
Atrial fibrillation currently afflicts over three million persons in the United States. [Cox et al., J. Thoracic. Cardiovas. Surg. 101:402-405 (1991)]. It is the most common sustained arrhythmia, increasing progressively in prevalence with advancing age, and occurring in 2%-4% of the population over the age of 60. Atrial fibrillation is associated with atherosclerosis, chronic rheumatic heart disease, and hypertensive heart disease. The medical treatment of atrial fibrillation is less than optimal in that it frequently fails to ablate the arrhythmia and is ultimately directed only toward the control of the ventricular response rate. This results in patients (1) continuing to experience the unpleasantness of an irregular heartbeat, (2) continuing to suffer the consequence of impaired hemodynamics because of loss of atrioventricular synchrony, and (3) remaining vulnerable to the thromboembolic complications of atrial fibrillation.
For example, certain antiarrhythmic drugs, like quinidine and procainamide, can reduce both the incidence and the duration of atrial fibrillation episodes. Yet, these drugs often fail to maintain sinus rhythm in the majority of patients. Atrio-venticular nodal blocking agent, e.g. drugs, like digitalis, Beta blockers, and calcium channel blockers, can also be given to control the ventricular response. However, many people are intolerant to such drugs. [Kerr, PACE 17:1203-1207 (1994)].
Nonpharmacologic tools to treat atrial fibrillation include atrial defibrillation, catheter ablation, and open heart surgery. While effective means of treatment, each possess unwanted drawbacks.
External electrical cardioversion/defibrillation has been an effective method for termination of atrial fibrillation. It has been a well-accepted mode of acute therapy for over thirty years. However, there is potential risk of myocardial damage, ventricular tachyarrhythmias, or thromboembolism with this technique. [Luderitz et al., Am. J. Cardiol. 77:45A-52A (1996)]. Most importantly, the procedure only terminates the event and does not treat the underlying problem.
Implantable atrial defibrillators have been used in patients recently. This method is accomplished by the implantation of an internal defibrillator and a nonthoractomy lead system. However, patients with frequent episodes of fibrillation or episodes of short duration and spontaneous termination are not good candidates and alternative methods of treatment must be attempted. Major problems involved with the implantation technique include the presence of continual pain, the risk of inducing ventricular tachycardia during low level shocks and rapid battery depletion. [Luderitz et al., Am. J. Cardiol. 77:45A-52A (1996)].
Ablation of the atrioventricular node (AV node) in patients with chronic or paroxysmal atrial fibrillation has been extensively described and provides relief in selected patients. The patient, however, is left in atrial fibrillation and therefore there is a persistent risk of thromboembolism and continued loss of contractile atrial function. This technique uses catheter ablation by radiofrequency energy to permanently disconnect the fibrillating atria from the ventricles. Pacing is then permanently provided to the ventricle. [Fritzpatrick et al., Am. Heart J. 131(3):499-507 (1996)]. In addition, radiofrequency catheter ablation has been used to create linear lesions in the right atrium. This technique uses a specially designed 14-polar catheter and results in the patient being free from arrhythmias or the need for medication for up to 3 months. Although encouraging results were obtained, the selection of patients that may utilize this specialized technique are very limited. Luderitz et al., Am. J. Cardiol. 77:45A-52A (1996)].
One open heart surgical procedure is the so-called "corridor" procedure. This approach separates the fibrillating atria from a strip of tissue connecting the sinus and the AV node. Because both right and left atria continue to fibrillate, the hemodynamic abnormalities associated with AF are not improved. In addition, the vulnerability to the development of left atrial thrombi is not alleviated. Originally, it was hypothesized that this small corridor of atrial tissue would not be large enough to sustain AF. However, AF may continue and anticoagulation remains necessary. [Luderitz et al., Am. J. Cardiol. 77:45A-52A (1996)].
Another open heart surgical procedure for treating atrial fibrillation, termed the "maze procedure", has been found to be effective in treating atrial fibrillation. The procedure makes a prescribed pattern of incisions to anatomically create a convoluted path, or maze, for electrical propagation within the left and right atria. The incisions direct the electrical impulse from the SA node along a specified route through both atria, resulting in a uniform contraction and therefore normal atrial transport function. The incisions finally direct the impulse to the AV node to activate the ventricles, restoring normal atrioventricular synchrony. The incisions are also carefully placed to interrupt the conduction routes of the common reentry circuits. Appropriately placed atrial incision not only (1) interrupt the conduction routes of the most common reentrant circuits, they also direct (2) the sinus impulse from the sinoatrial node to the AV node along a specified route and (3) preserve synchronous atrial electrical activation as a prerequisite for contraction. The maze procedure has been found effective in treating atrial fibrillation. Yet, despite its clinical success, the maze procedure is technically difficult to do and requires open heart surgery. Moreover, the procedure is not tailored to a specific patient and sometimes can result in a permanent loss of contractile atrial function. Because of these factors, only a few maze procedures are done each year. (U.S. Pat. No. 5,549,661 to Kordis et al., incorporated herein by reference).
What is needed presently is a safe method of treatment that is both cost effective and versatile enough to be used on a wide variety of cardiac diseases. The method would improve the patient's quality of life by allowing for increased performance of everyday tasks as well as providing a general satisfaction with overall health. In addition, it would lower the number of visits the cardiac patient must make to their physician, thus reducing health care costs. Also, the mortality rate for these patients will decline.